By Ciba Foundation Symposium 26

Chapter 1 Chairman's creation (pages 1–3): Alan S. Curry
Chapter 2 The Clinician's requisites from the Laboratory within the remedy of the Acutely Poisoned sufferer (pages 5–15): R. W. Newton
Chapter three The position of the Laboratory within the remedy of Narcotic Poisoning (pages 17–28): Vincent P. Dole
Chapter four Formation of Reactive Metabolites as a reason for Drug Toxicity (pages 29–55): James R. Gillette
Chapter five Separation and Detection of risky Metabolites of Amphetamines, Analgesics and Phenothiazines (pages 57–82): A. H. Beckett
Chapter 6 assessment of Chromatographic and Spectroscopic tactics (pages 83–103): A. C. Moffat
Chapter 7 Use of fuel Chromatography?Mass Spectrometry in Toxicological research (pages 105–124): Bo Holmstedt and Jan?Erik Lindgren
Chapter eight selection of hashish elements in Blood (pages 125–137): Stig Agurell
Chapter nine Drug Assay by way of Radioactive Reagents (pages 139–154): W. Riess
Chapter 10 An On?Line Liquid Chromatograph?Mass Spectrometer approach (pages 155–169): R. P. W. Scott, C. G. Scott, M. Munroe and J. Hess
Chapter eleven Luminescence equipment in Drug research (pages 171–192): J. W. Bridges
Chapter 12 Immunoassay of substances (pages 193–200): Irving Sunshine
Chapter thirteen Immunological equipment for Detecting medicines: their software within the Detection of Digitoxin, Digoxin and Morphine (pages 201–217): Charles W. Parker
Chapter 14 Drug research within the Overdosed sufferer (pages 219–238): B. Widdop
Chapter 15 The Morbid Anatomist's function in Drug Detection (pages 239–251): D. J. Gee
Chapter sixteen Drug?Induced Iatrogenic sickness: the chance of its Detection (pages 253–268): Henry Leach
Chapter 17 barriers of Haemodialysis and compelled Diuresis (pages 269–289): L. F. Prescott
Chapter 18 The Poisoned sufferer: The Clinician and the Laboratory (pages 291–314): Roy Goulding

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Although an increase in the proportion of unbound drug in plasma should not decrease clearance of the drug (rate of excretion/concentration of unbound drug) by glomerular filtration, it could decrease the urinary or biliary clearance by active transport systems in kidney or liver. For example, the clearance of highly bound drugs by active transport systems in kidney may exceed the blood flow rate through the kidney because the reversible drug-protein complexes dissociate as the concentration of unbound drug in plasma is decreased by the transport system.

M. & WITKOP,B. (1972) Experientia (Basel) 28,1129-1149 GILLETIE,J. R. (1973) in Toxicological Problems (Loomis, T. ), (Proc. V In?. Congr. , vol. 2), pp. Y. GLESDE,E. , JR. (1972) Biochem. Pharmacol. 21, 169-172 G R E E F. , STRIPP, B. & GILLETTE, J. R. (1969) Bwchem. Pharmacol. 18,1531-1533 JAGENBURG, 0. R. & TOCZKO, K. (1964) Biochem. J. , MITCHELL, J. , ZMAGLIONE, N. & GILLETTE, J. R. (1972) V In?. Congr. Pharmol. Abs. Vol. Papers 117, Karger, Basel JOLLOW, D. , MITCHELL, J. , P m , W. , DAVIS,D.

Furthermore, pretreatment of rats with phenobarbitone cannot increase the proportion converted into the epoxide and therefore should not have increased the covalent binding of bromobenzene epoxide to liver protein, even though pretreatment markedly increases the rate of bromobenzene metabolism. Instead, pretreatment with phenobarbitone should have caused a small decrease in covalent binding because it increases the activity of the epoxide hydrase (Daly et al. 1972). Indeed, phenobarbitone decreased the covalent binding of bromobenzene when low non-toxic doses of the toxicant were administered (Reid 1973; Reid & Krishna 1973).

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